Clinical infections caused by Enterococcus include urinary tract infections, bacteremia, bacterial endocarditis, diverticulitis, and meningitis. Sensitive strains of these bacteria can be treated with ampicillin and vancomycin. The most important feature of this genus is their high level of antibiotic resistance. In the last two decades, particularly virulent strains of Enterococcus which are resistant to vancomycin (Vancomycin-Resistant Enterococcus, or VRE) have emerged in nosocomial infections of hospitalized patients especially in the US.

Enterococcus faecium

Vancomycin-resistant enterococci (VRE) have caused hospital outbreaks worldwide, and the vancomycin-resistance gene (vanA) has crossed genus boundaries to methicillin-resistant Staphylococcus aureus. Spread of VRE, therefore, represents an immediate threat for patient care and creates a reservoir of mobile resistance genes for other, more virulent pathogens. Evolutionary genetics, population structure, and geographic distribution of 411 VRE and vancomycin-susceptible Enterococcus faecium isolates, recovered from human and nonhuman sources and community and hospital reservoirs in 5 continents, identified a genetic lineage of E. faecium (complex-17) that has spread globally. This lineage is characterized by 1) ampicillin resistance, 2) a pathogenicity island, and 3) an association with hospital outbreaks. Complex-17 is an example of cumulative evolutionary processes that improved the relative fitness of bacteria in hospital environments. Preventing further spread of this epidemic E. faecium subpopulation is critical, and efforts should focus on the early disclosure of ampicillin-resistant complex-17 strains.

Enterococcus faecium has become an important nosocomial [hospital-acquired] pathogen, especially in immunocompromised patients, creating serious limitations in treatment options because of cumulative resistance to antimicrobial agents. In the United States, the emergence of nosocomial E. faecium infections was characterized by increasing resistance to ampicillin in the 1980s and a rapid increase of vancomycin resistance in the next decade. The emergence of vancomycin-resistant E. faecium (VREF) in the United States illustrates the transmission capacities of bacteria and the possibility of a postantibiotic era for nosocomial infections in critically ill patients.

The global epidemiology of VREF is not well understood. In the United States, prevalences of colonization and infection are high among hospitalized patients, but a community reservoir of VREF in healthy persons or animals seems to be absent. In contrast, in Europe, colonization and infection rates within hospitals remain low, although colonization among healthy persons and animals is prevalent.

Enterococcus faecalis

Enterococcus faecalis is a commensal bacteria inhabiting the intestinal tracts of both humans and animals. Enterococcus faecalis is known to be capable of causing life-threatening infections in humans, particularly in the nosocomial [hospital] environment. The existence of enterococci in such a dual role is facilitated, at least in part, by its intrinsic and acquired resistance to virtually all antibiotics currently in use.

Enterococci are resistant to many commonly used antimicrobial agents (aminoglycosides, aztreonam, cephalosporins, clindamycin, the semi-synthetic penicillins nafcillin and oxacillin, and trimethoprim-sulfamethoxazole). Exposure to cephalosporins is a particularly important risk factor for colonization and infection with enterococci. Thus, the era in which safe and effective cephalosporins became widely available has also been an era of enterococcal ascendance.

E. faecalis can cause endocarditis, as well as bladder, prostate, and epididymal and nervous system infections.